Module 2 Flashcards
What is the onset of alcohol withdrawal
6-24 hours
Onset of DTs
48-72 hours
DT symptoms
Malignant HTN
Hyperthermia
LOC fluctations
Delerium
Alcohol withdrawal symptoms
increased BP increased temp increased HR tremors diaphoresis nausea and vomiting
First-line treatment for alcohol withdrawl
benzos
Sepsis
dysregulated host response to infection causing life-threatening organ dysfunction
Massive vasodilation
leaky vessels
decreased perfusion
using up clotting factors to make micro clots
septic shock
need for vasopressors to maintain map >65
Lactate > 2 despite fluid resus
SIRS
systemic inflammatory response system overwhelming unregulated inflammatory response resulting in: -uncontrolled coagulation -widespread vessel leakage -poor distribution of circulating volume
Goals of sepsis management (3)
early recognition
Manage BP
treat the cause (early abx)
Oxygen Dissociation curve
the ability of Hgb to bind with oxygen in the lungs and release oxygen to the tissues
Oxygen Dissociation curve shift LEFT
LOVE - High affinity
Hgb will pick up O2 readily from the lungs but holds on to it
results in decreased tissue perfusion/oxygenation
Oxygen Dissociation curve RIGHT
RELEASE- Low affinity
Hgb will pick up less O2 from the lungs but release it easily to tissues
results in decreased tissue perfusion/oxygenation
Causes of an Oxygen Dissociation curve shift LEFT
Decreased temp
Decreased H+ (high PH)
Decreased CO2 (hyperventilation)
Decreased 2-3 DPG
Causes of an Oxygen Dissociation curve shift RIGHT
Increased temp
Increased H+ (low PH)
Increased CO2 (hypoventilation)
Increased 2-3 DPG
Anaphylaxis vs allergic reaction
Anaphylaxis involves 2 or more body systems
State the hallmark symptoms of septic shock and brief patho
Warm, flushed skin - Exaggerated inflammatory response causing vasodilation
Depleted intravascular volume with normal total fluid volume , fluid distributed where it cant be accessed
Early malfunctioning of coagulation and depleted clotting factors = bleeding
Briefly describe the patho of sepsis
Bacteria in the blood causes release of endotoxins (gram neg) and exotoxins (gram pos) causing pro-inflammatory cytokines
Cytokines activate the complement and coagulation system, kinin system and neutrophils, monocyte/macrophage activity, causing more cytokines
Causes endothelial cell dysfunction causing vasodilation and vascular leaking
HIV disease Patho
Human immune deficiency virus
HIV targets and attacks WBC (primarily T helper (CD4) cells) by fusing to them and injecting its RNA
When infected T-helper cells die they release more replicated copies of HIV into the bloodstream
These take over more CD4 cells and within a few weeks the infected person experiences influenza-like symptoms as the body tries to fight the infection
as the viral load increases, there are few CD4 cells left to combat the disease and AIDS sets in
Role of T-helper cells (CD4)
T-helper cells (CD4) move through the body looking for and destroying viruses and germs
Latency stage
Viral replication stabilizes and the immune system is able to reduce viral levels
this can last up to a decade
AIDS
final stage of HIV
Severe state of immunodeficiency
Norm CD4 count
500-1500
<200 = aids
Viral load
How much HIV RNA is in a persons blood
the higher the viral load the more HIV symptoms a person will expirence
HIV symptoms
Rash
Pneumonia
Peripheral neuropathy
LOC changes
HAART
Highly active antiretroviral therapy (HAART) is a medication regimen used to manage and treat HIV
Normal Inflammatory response
Mast cells release histamines
Histamines cause vasodilation and vascular permeability
Vascular permeability is needed to bring the key players to the site of infection
Neutrophils (phagocytes) are recruited
Platelets recruited and clotting starts
Lactate
Released when cells arent getting enough oxygen
Biproduct of anaerobic metabolism when cells don’t have enough O2 they create energy with out it and lactate is the byproduct
norm <2
Fluid resuscitation in adults
30cc/KG
Things that impact oxygen supply
Cardiac output
Hemoglobin
Arterial O2
ventilation
Things that impact oxygen demand
Tachycardia
Fever
Activity
Stress
Cardiac output in sepsis
Decreased preload due to decreased circulating volume
Decreased afterload due to dilated vessels
increased myocardial oxygen demand and decreased supply causes decreased contractility
Chronotropes:
drugs that change the heart rate, some may also change heart rhythm
Inotropes:
Inotropes change the contractile force of the heart. Positive inotropes increase contractile force.
Negative inotropes decrease the contractile force
Beta 2:
Beta2- lungs bronchiodilation
Beta 1:
Beta 1 receptors- heart.
increases cardiac output and stroke volume by increasing heart rate, contractility.
Alpha 1:
Activation of alpha 1 adrenergic receptors cause smooth muscle contraction which induces vasoconstriction.
Phenylephrine
Acts quickly to squeeze the pipes
Vasopressin
alpha 1- vasoconstriction
Dobutamine
positive inotrope- increases contractility
Primary used for cardiogenic shock
Epinephrine
works on alpha 1 and beta 1 and beta 2
Alpha 1- vasoconstriction
Beta 1 increases contractility
Beta 2- Bronchiodilation
Norepinephrine
potent Vassopressor
used for sepsis and trauma
Dopamine
Inotropic increases contractility and vassopressor
good for cardiogenic shock with hypotension
